Clogging of the drainage layer is the main reason for the inefficiency and failure of the leachate collection system in municipal solid waste (MSW) landfills. One of the most important challenges in the design and operation of landfills is to identify the factors affecting the drainage layer clogging and the extent of their influence especially in the real scale. In this study, five experimental columns were designed to investigate the effective factors on the clogging of the drainage system in the MSW landfills, making it possible to measure the effect of different parameters on the drainage layer clogging through simulating the real conditions. The designed columns are capable to apply the boundary conditions of the MSW landfill including temperature, pressure, and leachate recirculation as well as measuring the permeability of drainage layer. High strength real leachate recirculated in the experimental columns to monitor the degree of drainage layer clogging through the regular measurement of permeability in the different columns. The results showed hydraulic conductivity of the drainage layer decreased between 20 to 50 percent in different samples over time. Although the particle size of drainage materials directly influences the reduction of hydraulic conductivity, the common concentration of calcium carbonate in the materials of the drainage layer does not considerably affect this issue. Formation of biofilm in the drainage layer was observed through scanning electron microscope (SEM) and visual inspection in all columns indicating the proper performance of clogging process simulator which is designed and developed in this research.

The present study aims at determining the geotechnical properties of the tailings and the natural bed at Iran Mineral Processing Company, Sites 1 and 5. It qualitatively studies the subsurface layers of the company’s tailings storage site. After drilling different boreholes and conducting in-situ tests, it has made laboratory analyses in the form of field exploration to determine the geotechnical parameters of the extracted samples. Results from the analyses show the permeability coefficient of the subsurface layer of Site No. 1 and 5 to be very small, in the range of 10-7 cm/sec. Considering the conformity of permeability coefficient, percentage of fine grains (98% to 99%), plasticity index (28.5-29.5), and clay content of different layers of Sites 1 and 5 (68%-80%), based on the compacted clay liner criteria, it can be concluded that by nature, the subsurface layers of the mentioned sites are sealed with no need for any compacted clay liner. The tailings for storage Site 5 are fine-grained (80-88<75mm), basically in ML range according to USCS system, with a permeability coefficient of about 10-6 cm/sec. Therefore, the tailings themselves act as a relatively primary sealing layer against the infiltration of hazardous leachates into the natural bed. The method, used in the process of site selection of tailings storage facilities (TSF), can cut the construction time as well as the expenditures, thus reducing the production costs in the long run.

In recent years, the cardiovascular toxicity of urban fine particulate matter (PM₂.₅) has sparked significant alarm. Mitochondria produce 90% of ATP and make up 30% of the volume of cardiomyocytes. Thus knowledge of myocardial mitochondrial dysfunction due to PM₂.₅ exposure is essential for further cardiotoxic effects. Here, the mechanism of PM₂.₅-induced cardiac hypertrophy through calcium overload and mitochondrial dysfunction was investigated in vivo and in vitro. Male and female BALB/c mice were given 1.28, 5.5, and 11 mg PM₂.₅/kg bodyweight weekly through oropharyngeal inhalation for four weeks and were assigned to low, medium, and high dose groups, respectively. PM₂.₅-induced myocardial edema and cardiac hypertrophy were detected in the high-dose group. Mitochondria were scattered and ruptured with abnormal ultrastructural morphology. In vitro experiments on human cardiomyocyte AC16 showed that exposure to PM₂.₅ for 24 h caused opened mitochondrial permeability transition pore --leading to excessive calcium production, decreased mitochondrial membrane potential, weakened mitochondrial respiratory metabolism capacity, and decreased ATP production. Nevertheless, the administration of calcium chelator ameliorated the mitochondrial damage in the PM₂.₅-treated group. Our in vivo and in vitro results confirmed that calcium overload under PM₂.₅ exposure triggered mTOR/AKT/GSK-3β activation, leading to mitochondrial bioenergetics dysfunction and cardiac hypertrophy.

Xanthan gels were assessed to control the reductive dechlorination of hexachlorocyclohexanes (HCHs) and trichlorobenzenes (TCBs) in a strong permeability contrast and high velocity sedimentary aquifer. An alkaline degradation was selected because of the low cost of NaOH and Ca(OH)₂. The rheology of alkaline xanthan gels and their ability to deliver alkalinity homogeneously, while maintaining the latter, were studied. Whereas the xanthan gels behaved like non-Newtonian shear-thinning fluids, alkalinity and Ca(OH)₂ microparticles had detrimental effects, yet, the latter decreased with the shear-rate. Breakthrough curves for the NaOH and Ca(OH)₂ in xanthan solutions, carried out in the lowest permeability soil (9.9 μm²), demonstrated the excellent transmission of alkalinity, while moderate pressure gradients were applied. Injection velocities ranging from 1.8 to 3.8 m h⁻¹ are anticipated in the field, given the permeability range from 9.9 to 848.7 μm². Despite a permeability contrast of 8.7 in an anisotropic aquifer model, the NaOH and the Ca(OH)₂ both in xanthan gels spread only 5- and 7-times faster in the higher permeability zone, demonstrating that the delivery was enhanced. Moreover, the alkaline gels which were injected into a high permeability layer under lateral water flow, showed a persistent blocking effect and longevity (timescale of weeks), in contrast to the alkaline solution in absence of xanthan. Kinetics of alkaline dechlorination carried out on the historically contaminated soil, using the Ca(OH)₂ suspension in xanthan solution, showed that HCHs were converted in TCBs by dehydrodechlorination, whereas the latter were then degraded by reductive hydrogenolysis. Degradation kinetics were achieved within 30 h for the major and most reactive fraction of HCHs.

The surface modifications of nanoparticles (NPs), are well-recognized parameters that affect the toxicity, while there has no study on toxicity of Al₂O₃ NPs with different surface modification. Therefore, for the first time, this study pays attention to evaluating the toxicity and potential mechanism of pristine Al₂O₃ NPs (p-Al₂O₃), hydrophilic (w-Al₂O₃) and lipophilic (o-Al₂O₃) modifications of Al₂O₃ NPs both in vitro and in vivo. Applied concentrations of 10, 20, 40, 80,100 and 200 μg/mL for 24 h exposure on Caenorhabditis elegans (C. elegans), while 100 μg/mL of Al₂O₃ NPs significantly decreased the survival rate. Using multiple toxicological endpoints, we found that o-Al₂O₃ NPs (100 μg/mL) could induce more severe toxicity than p-Al₂O₃ and w-Al₂O₃ NPs. After uptake by C. elegans, o-Al₂O₃ NPs increased the intestinal permeability, easily swallow and further destroy the intestinal membrane cells. Besides, cytotoxicity evaluation revealed that o-Al₂O₃ NPs (100 μg/mL) are more toxic than p-Al₂O₃ and w-Al₂O₃. Once inside the cell, o-Al₂O₃ NPs could attack mitochondria and induce the over-production of reactive oxygen species (ROS), which destroy the intracellular redox balance and lead to apoptosis. Furthermore, the transcriptome sequencing and RT-qPCR data also demonstrated that the toxicity of o-Al₂O₃ NPs is highly related to the damage of cell membrane and the imbalance of intracellular redox. Generally, our study has offered a comprehensive sight to the adverse effects of different surface modifications of Al₂O₃ NPs on environmental organisms and the possible underlying mechanisms.

Microcystin-LR (MC-LR) and glyphosate (GLY) have been classified as a Group 2B and Group 2A carcinogens for humans, respectively, and frequently found in aquatic ecosystems. However, data on the potential hazard of MC-LR and GLY exposure to the fish gut are relatively scarce. In the current study, a subacute toxicity test of zebrafish exposed to MC-LR (35 μg L⁻¹) and GLY (3.5 mg L⁻¹), either alone or in combination was performed for 21 d. The results showed that MC-LR or/and GLY treatment reduced the mRNA levels of tight junction genes (claudin-5, occludin, and zonula occludens-1) and altered the levels of diamine oxidase and D-lactic, indicating increased intestinal permeability in zebrafish. Furthermore, MC-LR and/or GLY treatment remarkably increased the levels of intestinal IL-1β and IL-8 but decreased the levels of IL-10 and TGF-β, indicating that MC-LR and/or GLY exposure induced an inflammatory response in the fish gut. MC-LR and/or GLY exposure also activated superoxide dismutase and catalase, generally upregulated the levels of p53, bax, bcl-2, caspase-3, and caspase-9, downregulated the levels of caspase-8 and caused notable histological injury in the fish gut. Moreover, MC-LR and/or GLY exposure also significantly altered the microbial community in the zebrafish gut and the expression of miRNAs (miR-146a, miR-155, miR-16, miR-21, and miR-223). Chronic exposure to MC-LR and/or GLY can induce intestinal damage in zebrafish, and this study is the first to demonstrate an altered gut microbiome and miRNAs in the zebrafish gut after MC-LR and GLY exposure.

Pendimethalin (PDM) is a dinitroaniline crop pesticide that is extensively utilized worldwide. However, the reproductive toxicity and cellular mechanisms of PDM have not been identified. Therefore, we elucidated the adverse effects of PDM on the reproductive system using mouse testicular Leydig and Sertoli cells (TM3 and TM4 cells, respectively). Our results demonstrated that PDM suppressed the viability and proliferation of TM3 and TM4 cells. Additionally, PDM induced cytosolic calcium upregulation and permeabilization of mitochondrial membrane potential in both TM3 and TM4 cells. We also verified that PDM activates the endoplasmic reticulum (ER) stress pathway and autophagy. Furthermore, we confirmed that activation of ER stress and autophagy were blocked by 2-aminoethoxydiphenyl borate (2-APB) treatment. Finally, we confirmed PDM-induced cell cycle arrest and apoptosis in TM3 and TM4 cells. Thus, we first demonstrated that PDM impedes the survival of testis cells, and further, their function.

Hydraulic fracturing of horizontal wells is a cost effective means for extracting oil and gas from low permeability formations. Hydraulic fracturing often produces considerable volumes of flowback and produced water (FPW). FPW associated with hydraulic fracturing has been shown to be a complex, often brackish mixture containing a variety of anthropogenic and geogenic compounds. In the present study, the risk of FPW releases to aquatic systems was studied using the model benthic invertebrate, Lumbriculus variegatus and field-collected FPW from a fractured well in Alberta. Acute, chronic, and pulse toxicity were evaluated to better understand the implications of accidental FPW releases to aquatic environments. Although L.variegatus is thought to have a high tolerance to many stressors, acute toxicity was significant at low concentrations (i.e. high dilutions) of FPW (48 h LC50: 4–5%). Chronic toxicity (28 d)of FPW in this species was even more pronounced with LC50s (survival/reproduction) and EC50s (total mass) at dilutions as low as 0.22% FPW. Investigations evaluating pulse toxicity (6 h and 48 h exposure) showed a significant amount of latent mortality occurring when compared to the acute results. Additionally, causality in acute and chronic bioassays differed as acute toxicity appeared to be primarily driven by salinity, which was not the case for chronic toxicity, as other stressors appear to be important as well. The findings of this study show the importance of evaluating multiple exposure regimes, the complexity of FPW, and also shows the potential aquatic risk posed by FPW releases.

In-site remediation is a relatively promising and socially acceptable technique for heavy metal contaminated soils. But the key task is to select cost-effective and environment-friendly amendents for the consideration of practical application. Based on the property of four typical silicate wastes such as straw ash (SA), coal fly ash (CFA), ferronickel slag (FNS) and blast-furnace slag (BFS), effects of four wastes on available Cd content and Cd chemical speciation in amended soils, and physicochemical properties of the amended soils were carried out in the study. The results showed that four wastes were dominately composed of the amorphous phases with OH⁻ ions readily released. When the weight ratio of silicate wastes to artificial Cd-contaminated soils reached 10%, the available Cd contents decreased from 4.12 mg/kg in untreated soils to 1.94, 1.92, 1.45 and 1.53 mg/kg in amended soils by adding SA, CFA, FNS and BFS respectively, after the soils were amended for 30 days. The residual fraction of Cd (R) was 2.54, 2.48, 2.77 and 2.58 times higher in amended soil than that in untreated soil when SA, CFA, FNS and BFS was added, respentively. The soil pH and CEC were improved. The amended soils by adding SA and FNS were looser than those by adding CFA and BFS, and air permeability of the amended soils by SA was better than that by FNS.

Interactions between the intestine and the liver, the so-called ‘gut-liver axis’, play a crucial role in the onset of hepatic steatosis and non-alcoholic fatty liver disease. However, not much is known about the impact of environmental pollutants on the gut-liver axis and consequent hepatic steatosis. Bisphenol A (BPA), a widely used plasticiser, is an important environmental contaminant that affects gut microbiota. We hypothesised that BPA induces hepatic steatosis by promoting gut microbiota dysbiosis and activating the gut-liver axis. In this study, male CD-1 mice were fed with diet containing BPA (50 μg/kg body weight/day) for 24 weeks. Dietary exposure to BPA increased lipid contents and fat accumulation in the liver. Analysis of 16 S rRNA gene sequencing revealed that the diversity of gut microbiota reduced and the composition of gut microbiota was altered in the BPA-fed mice. Further, the abundance of Proteobacteria, a marker of dysbacteria, increased, whereas the abundance of Akkermansia, a gut microbe associated with increased gut barrier function and reduced inflammation, markedly decreased. Expression levels of intestinal tight junction proteins (zona occludens-1 and occludin) also decreased drastically, leading to increased intestinal permeability and elevated levels of endotoxins. Furthermore, BPA up-regulated the expression of Toll-like receptor 4 (TLR4) and phosphorylation of nuclear factor-kappa B (NF-κB) in the liver and increased the production of inflammatory cytokines, including interleukin-1β, interleukin-18, tumour necrosis factor-α, and interleukin-6. Take together, our work indicated that dietary intake of BPA induced hepatic steatosis, and this was closely related to dysbiosis of gut microbiota, elevated endotoxin levels, and increased liver inflammation through the TLR4/NF-κB pathway.